ARTICLE
Auteur(s) : Selda Pelin
Kartal Durmazlar, Bilgen Oktay, Cemile Eren, Fatma Eskioglu
Department of Dermatology, Ministry of Health Ankara
Diskapi Yildirim Beyazit Education and Research Hospital,
Ankara, Turkey
A 28-year-old woman presented with generalized erythroderma and
clear signs of Cushing’s syndrome (figure 1A). She had been
well until two months previously when she developed generalized
erythrodermic psoriasis, for which she was prescribed oral
50 mg/day acitretin and topical mometasone furoate 0.1%
ointment 50 g/week.
She was 152 cm tall, weighed 62 kg and her blood
pressure was 140/95 mmHg. Her general laboratory findings were
within normal limits except for slightly elevated cholesterol.
Initial endocrinological investigations showed morning cortisol at
4.74 μg/dL (normal 5-25 μg/dL), adrenocorticotropic hormone
(ACTH) level lower than 5 pg/mL (normal 5-46 pg/mL) and three
consecutive 24-hour urinary free cortisol levels lower than
4 μg/24 h. Magnetic resonance imaging of the pituitary
gland and abdomen showed no abnormality. While acitretin
50 mg/day therapy was continuing, we stopped the application
of topical corticosteroid to perform the ACTH stimulation test.
Subsequently, the patient developed abdominal pain, high fever,
nausea, loss of appetite, weakness, fatigue with a blood pressure
of 95/55 mmHg, leukocytosis and evidence of a urinary tract
infection. Intravenous 200 mg/day hydrocortisone was
administered immediately as a stress dose for adrenal insufficiency
and an antibiotic medication was commenced for the urinary tract
infection. Three days later the stress dose steroid was switched to
dexamethasone and 1 μg ACTH was given and cortisol levels were
drawn at 0, 30, and 60 minutes. Cortisol levels were found
suppressed as follows: 3 μg/dL, 4.2 μg/dL, and 5.1 μg/dL.
A normal cortisol response to low-dose ACTH test is accepted
as a peak of greater than 20 μg/dL. Iatrogenic Cushing’s
syndrome was diagnosed.
To determine the cause of the Cushing’s syndrome and adrenal
suppression, we took a detailed drug history from the patient and
contacted her doctors, pharmacists and relatives. She had never
taken systemic glucocorticoids and had used only the 50 g/week
of mometasone furoate prescribed. She and her family denied
exceeding this dose or using any other product that may have
inhibited glucocorticoid metabolism. It was confirmed that the
Cushingoid features had developed only in the 2 months since
starting the mometasone furoate.
After one week, we switched to oral prednisolone and gradually
tapered over two months. The acitretin dose was reduced to
25 mg/day. Three months later, the patient’s weight had
decreased to 55 kg and the features of Cushing’s syndrome had
become less evident (figure 1B).
Discussion
The duration, dosage and the choice of the potency, together with
an individual susceptibility, determine the occurrence of the
adverse effects of glucocorticoids [1] For prevention, the use of
less than 50 g per week of potent glucocorticoids has been
suggested [2]. However, plasma cortisol levels are easily
suppressed by the most potent preparations after only a few days
[2]. So, intensive topical glucocorticoid application should be
slightly tapered. Treatment failure has been shown to correlate
with prescription of high potency glucocorticoids in psoriasis [3].
An increase in glucocorticoid penetration has been shown to augment
the potential for hypothalamic-pituitary-adrenal axis suppression
[2]. Instances of low-potency topical glucocorticoids causing
systemic side effects in patients with abnormal barrier function
have been reported [4]. Subtle changes occur in the epidermal
barrier upon topical glucocorticoid application, as evidenced by
delayed barrier recovery [5]. The minimum glucocorticoid dosage
required for an adequate clinical response varies among
individuals. Potential markers for glucocorticoid sensitivity at
the cellular level have been reported [6]. Apart from individual
susceptibility, the concomitant usage of acitretin might have
contributed to the altered barrier function and increased
absorption in our patient, and the use of glucocorticoids might
have worsened the barrier impairment. The presentation of our case
is a reminder of the risk of using topical glucocorticoids in
erythrodermic patients.
Acknowledgements
Conflict of interest: none. Financial support: none.
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